Longitudinal assessment of von Willebrand factor antigen and von Willebrand factor propeptide in response to alteration of antiplatelet therapy after TIA or ischaemic stroke

William Tobin, J. A. Kinsella, G. F. Kavanagh, J. S. O'Donnell, R. T. McGrath, T. Coughlan, D. R. Collins, D. O'Neill, B. Egan, S. Tierney, T. M. Feeley, R. P. Murphy, D. J H McCabe

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

The impact of commencing or changing antiplatelet therapy on von Willebrand factor antigen (VWF:Ag) and von Willebrand factor propeptide (VWF:Ag II) levels has not been comprehensively assessed following TIA or ischaemic stroke. In this pilot, longitudinal, observational analytical study, VWF:Ag and VWF:Ag II levels were simultaneously quantified in platelet poor plasma by ELISA in patients within 4 weeks of TIA or ischaemic stroke (baseline), and then 14 days (14d) and >90 days (90d) after altering antiplatelet therapy. Ninety-one patients were recruited. Eighteen were initially assessed on no antiplatelet therapy, and then after 14d (N = 17) and 90d (N = 8) on aspirin monotherapy; 21 patients were assessed on aspirin and after 14d and 90d on clopidogrel; 52 were assessed on aspirin monotherapy, and after 14d and 90d on aspirin and dipyridamole combination therapy. VWF:Ag, VWF:Ag II levels and VWF:Ag/VWF:Ag II ratio were unchanged at 14d and 90d in the overall study population (p ≥0.1). VWF:Ag and VWF:Ag II levels remained stable at 14d and 90d after commencing aspirin (p ≥0.054), and after changing from aspirin to clopidogrel (p ≥0.2). Following the addition of dipyridamole MR to aspirin, there was a significant reduction in VWF:Ag levels at 14d (p = 0.03) and 90d (p = 0.005), but not in VWF:Ag II levels (p ≥0.3). The addition of dipyridamole to aspirin led to a persistent reduction in VWF:Ag but not in VWF:Ag II levels, suggesting that dipyridamole may inhibit release of platelet-derived VWF:Ag following TIA or ischaemic stroke.

Original languageEnglish (US)
Pages (from-to)1405-1412
Number of pages8
JournalJournal of Neurology
Volume261
Issue number7
DOIs
StatePublished - 2014
Externally publishedYes

Fingerprint

von Willebrand Factor
Stroke
Aspirin
Dipyridamole
clopidogrel
Therapeutics
Von Willebrand antigen
Blood Platelets
Observational Studies

Keywords

  • Aspirin
  • Clopidogrel
  • Dipyridamole
  • High on treatment platelet reactivity
  • Stroke
  • TIA
  • von Willebrand factor
  • von Willebrand factor propeptide

ASJC Scopus subject areas

  • Clinical Neurology
  • Neurology
  • Medicine(all)

Cite this

Longitudinal assessment of von Willebrand factor antigen and von Willebrand factor propeptide in response to alteration of antiplatelet therapy after TIA or ischaemic stroke. / Tobin, William; Kinsella, J. A.; Kavanagh, G. F.; O'Donnell, J. S.; McGrath, R. T.; Coughlan, T.; Collins, D. R.; O'Neill, D.; Egan, B.; Tierney, S.; Feeley, T. M.; Murphy, R. P.; McCabe, D. J H.

In: Journal of Neurology, Vol. 261, No. 7, 2014, p. 1405-1412.

Research output: Contribution to journalArticle

Tobin, W, Kinsella, JA, Kavanagh, GF, O'Donnell, JS, McGrath, RT, Coughlan, T, Collins, DR, O'Neill, D, Egan, B, Tierney, S, Feeley, TM, Murphy, RP & McCabe, DJH 2014, 'Longitudinal assessment of von Willebrand factor antigen and von Willebrand factor propeptide in response to alteration of antiplatelet therapy after TIA or ischaemic stroke', Journal of Neurology, vol. 261, no. 7, pp. 1405-1412. https://doi.org/10.1007/s00415-014-7362-3
Tobin, William ; Kinsella, J. A. ; Kavanagh, G. F. ; O'Donnell, J. S. ; McGrath, R. T. ; Coughlan, T. ; Collins, D. R. ; O'Neill, D. ; Egan, B. ; Tierney, S. ; Feeley, T. M. ; Murphy, R. P. ; McCabe, D. J H. / Longitudinal assessment of von Willebrand factor antigen and von Willebrand factor propeptide in response to alteration of antiplatelet therapy after TIA or ischaemic stroke. In: Journal of Neurology. 2014 ; Vol. 261, No. 7. pp. 1405-1412.
@article{e441e1223ea544de87589b9445a58d76,
title = "Longitudinal assessment of von Willebrand factor antigen and von Willebrand factor propeptide in response to alteration of antiplatelet therapy after TIA or ischaemic stroke",
abstract = "The impact of commencing or changing antiplatelet therapy on von Willebrand factor antigen (VWF:Ag) and von Willebrand factor propeptide (VWF:Ag II) levels has not been comprehensively assessed following TIA or ischaemic stroke. In this pilot, longitudinal, observational analytical study, VWF:Ag and VWF:Ag II levels were simultaneously quantified in platelet poor plasma by ELISA in patients within 4 weeks of TIA or ischaemic stroke (baseline), and then 14 days (14d) and >90 days (90d) after altering antiplatelet therapy. Ninety-one patients were recruited. Eighteen were initially assessed on no antiplatelet therapy, and then after 14d (N = 17) and 90d (N = 8) on aspirin monotherapy; 21 patients were assessed on aspirin and after 14d and 90d on clopidogrel; 52 were assessed on aspirin monotherapy, and after 14d and 90d on aspirin and dipyridamole combination therapy. VWF:Ag, VWF:Ag II levels and VWF:Ag/VWF:Ag II ratio were unchanged at 14d and 90d in the overall study population (p ≥0.1). VWF:Ag and VWF:Ag II levels remained stable at 14d and 90d after commencing aspirin (p ≥0.054), and after changing from aspirin to clopidogrel (p ≥0.2). Following the addition of dipyridamole MR to aspirin, there was a significant reduction in VWF:Ag levels at 14d (p = 0.03) and 90d (p = 0.005), but not in VWF:Ag II levels (p ≥0.3). The addition of dipyridamole to aspirin led to a persistent reduction in VWF:Ag but not in VWF:Ag II levels, suggesting that dipyridamole may inhibit release of platelet-derived VWF:Ag following TIA or ischaemic stroke.",
keywords = "Aspirin, Clopidogrel, Dipyridamole, High on treatment platelet reactivity, Stroke, TIA, von Willebrand factor, von Willebrand factor propeptide",
author = "William Tobin and Kinsella, {J. A.} and Kavanagh, {G. F.} and O'Donnell, {J. S.} and McGrath, {R. T.} and T. Coughlan and Collins, {D. R.} and D. O'Neill and B. Egan and S. Tierney and Feeley, {T. M.} and Murphy, {R. P.} and McCabe, {D. J H}",
year = "2014",
doi = "10.1007/s00415-014-7362-3",
language = "English (US)",
volume = "261",
pages = "1405--1412",
journal = "Journal of Neurology",
issn = "0340-5354",
publisher = "D. Steinkopff-Verlag",
number = "7",

}

TY - JOUR

T1 - Longitudinal assessment of von Willebrand factor antigen and von Willebrand factor propeptide in response to alteration of antiplatelet therapy after TIA or ischaemic stroke

AU - Tobin, William

AU - Kinsella, J. A.

AU - Kavanagh, G. F.

AU - O'Donnell, J. S.

AU - McGrath, R. T.

AU - Coughlan, T.

AU - Collins, D. R.

AU - O'Neill, D.

AU - Egan, B.

AU - Tierney, S.

AU - Feeley, T. M.

AU - Murphy, R. P.

AU - McCabe, D. J H

PY - 2014

Y1 - 2014

N2 - The impact of commencing or changing antiplatelet therapy on von Willebrand factor antigen (VWF:Ag) and von Willebrand factor propeptide (VWF:Ag II) levels has not been comprehensively assessed following TIA or ischaemic stroke. In this pilot, longitudinal, observational analytical study, VWF:Ag and VWF:Ag II levels were simultaneously quantified in platelet poor plasma by ELISA in patients within 4 weeks of TIA or ischaemic stroke (baseline), and then 14 days (14d) and >90 days (90d) after altering antiplatelet therapy. Ninety-one patients were recruited. Eighteen were initially assessed on no antiplatelet therapy, and then after 14d (N = 17) and 90d (N = 8) on aspirin monotherapy; 21 patients were assessed on aspirin and after 14d and 90d on clopidogrel; 52 were assessed on aspirin monotherapy, and after 14d and 90d on aspirin and dipyridamole combination therapy. VWF:Ag, VWF:Ag II levels and VWF:Ag/VWF:Ag II ratio were unchanged at 14d and 90d in the overall study population (p ≥0.1). VWF:Ag and VWF:Ag II levels remained stable at 14d and 90d after commencing aspirin (p ≥0.054), and after changing from aspirin to clopidogrel (p ≥0.2). Following the addition of dipyridamole MR to aspirin, there was a significant reduction in VWF:Ag levels at 14d (p = 0.03) and 90d (p = 0.005), but not in VWF:Ag II levels (p ≥0.3). The addition of dipyridamole to aspirin led to a persistent reduction in VWF:Ag but not in VWF:Ag II levels, suggesting that dipyridamole may inhibit release of platelet-derived VWF:Ag following TIA or ischaemic stroke.

AB - The impact of commencing or changing antiplatelet therapy on von Willebrand factor antigen (VWF:Ag) and von Willebrand factor propeptide (VWF:Ag II) levels has not been comprehensively assessed following TIA or ischaemic stroke. In this pilot, longitudinal, observational analytical study, VWF:Ag and VWF:Ag II levels were simultaneously quantified in platelet poor plasma by ELISA in patients within 4 weeks of TIA or ischaemic stroke (baseline), and then 14 days (14d) and >90 days (90d) after altering antiplatelet therapy. Ninety-one patients were recruited. Eighteen were initially assessed on no antiplatelet therapy, and then after 14d (N = 17) and 90d (N = 8) on aspirin monotherapy; 21 patients were assessed on aspirin and after 14d and 90d on clopidogrel; 52 were assessed on aspirin monotherapy, and after 14d and 90d on aspirin and dipyridamole combination therapy. VWF:Ag, VWF:Ag II levels and VWF:Ag/VWF:Ag II ratio were unchanged at 14d and 90d in the overall study population (p ≥0.1). VWF:Ag and VWF:Ag II levels remained stable at 14d and 90d after commencing aspirin (p ≥0.054), and after changing from aspirin to clopidogrel (p ≥0.2). Following the addition of dipyridamole MR to aspirin, there was a significant reduction in VWF:Ag levels at 14d (p = 0.03) and 90d (p = 0.005), but not in VWF:Ag II levels (p ≥0.3). The addition of dipyridamole to aspirin led to a persistent reduction in VWF:Ag but not in VWF:Ag II levels, suggesting that dipyridamole may inhibit release of platelet-derived VWF:Ag following TIA or ischaemic stroke.

KW - Aspirin

KW - Clopidogrel

KW - Dipyridamole

KW - High on treatment platelet reactivity

KW - Stroke

KW - TIA

KW - von Willebrand factor

KW - von Willebrand factor propeptide

UR - http://www.scopus.com/inward/record.url?scp=84904881513&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84904881513&partnerID=8YFLogxK

U2 - 10.1007/s00415-014-7362-3

DO - 10.1007/s00415-014-7362-3

M3 - Article

C2 - 24781842

AN - SCOPUS:84904881513

VL - 261

SP - 1405

EP - 1412

JO - Journal of Neurology

JF - Journal of Neurology

SN - 0340-5354

IS - 7

ER -